4. drug therapy Flashcards
DRUG THERAPY
Is the most common treatment for schizophrenia and includes the use of
antipsychotic drugs (a person with psychosis experiences some loss of contact with reality through hallucinations and delusions. It is a defining characteristic of schizophrenia and related disorders.)
CHLORPROMAZINE
This normalises neurotransmission in key areas of the brain, reducing symptoms like?
hallucinations (caused by hyperdopaminergia).
It also has a sedative effect (related to its effect on histamine receptors) and it is used to calm individuals when they are first admitted to hospitals.
TYPICAL ANTIPSYCHOTICS (1950S)
CHLORPROMAZINE: acts as an antagonist in the dopamine system and
blocks dopamine receptors in the synapses of the brain, reducing the action of dopamine this initially increases dopamine levels then reduces its production.
ATYPICAL ANTIPSYCHOTICS (1970S /90S)
Were developed to overcome the issues of the side effects of typical antipsychotics.
CLOZAPINE:
binds to dopamine receptors in the same way that chlorpromazine does, but also acts on serotonin and glutamate receptors helps improve mood, reducing depression and anxiety in patients (30-50% of people with schizophrenia attempt suicide at some point).
It is used when all other treatments fail.
RISPERIDONE: an attempt to produce a drug as effective as clozapine with fewer side effects. Binds to
both dopamine and serotonin receptors binds to dopamine receptors more strongly than clozapine so it is much more effective in smaller doses, leading to fewer side effects.
Chlorpromazine
1. DATE DEVELOPED
1. TYPICAL DOSAGE
1. TAKEN THROUGH
1. BINDS TO
1. SIDE EFFECTS
- 1950s
- 400-800mg. Up to 1000mg
- Tablet, liquid, injection
- Dopamine receptors
- Sedation, dizziness, weight gain. Long term uses tardive dyskinesia (involuntary facial movements e.g. grimacing).
Most serious side effect neuroleptic malignant syndrome (NMS) resulting in a high temperature and a coma (can be fatal - up to 2% of patients)
Clozapine
1. DATE DEVELOPED
1. TYPICAL DOSAGE
1. TAKEN THROUGH
1. BINDS TO
1. SIDE EFFECTS
- 1970s
- 300mg Up to 450mg
- Tablet
- Dopamine, serotonin, glutamate
- Dizziness, nausea, headaches,
Most serious side effect agranulocytosis (lowered blood cells) can cause increased risk of infections (users must take blood tests regularly).
Risperidone
1. DATE DEVELOPED
1. TYPICAL DOSAGE
1. TAKEN THROUGH
1. BINDS TO
1. SIDE EFFECTS
- 1990s
- 4-8 mg Up to 12 mg
- Tablet, liquid, injection
- Dopamine, serotonin.
- Agitation, anxiety, blurred vision.
AO3: strength of biological therapy
RESEATCH SUPPORT - Thornley
There is a large body of evidence to support that both atypical and typical antipsychotics are at least moderately effective in tackling the symptoms of schizophrenia.
Thornley et al. reviewed studies comparing the effects of chlorpromazine to control conditions. Data from 13 trials with a total of 1121 participants showed that it was associated with better overall functioning and reduced symptom severity as compared to a placebo. Furthermore, Meltzer concluded that clozapine is more effective than typical antipsychotics, it is effective in 30-50% of treatment resistant cases where typical antipsychotics have failed.
This means that both typical and atypical antipsychotics work.
AO3: limitation of biological therapy
side effects
There is a high likelihood of side effects.
Typical antipsychotics are associated with dizziness, weight gain and sleepiness. Long term use can result in tardive dyskinesia caused by dopamine super sensitivity and causes involuntary facial movements such as grimacing. The most serious side effect, neuroleptic malignant syndrome (NMS) is caused when the drug blocks dopamine action in the hypothalamus, an area in the brain associated with the regulation of several body systems. NMS results in a high temperature, a coma and can be fatal, affecting up to 2% of patients.
This means that antipsychotics can do harm as well as good, and individuals who experience these side effects may choose not to take it and relapse
AO3: limitation of biological therapy
MECHANISM UNCLEAR
We do not know why antipsychotics work.
Our understanding of the mechanism by which antipsychotics work is strongly tied up with the original dopamine hypothesis (symptoms are linked to high levels of dopamine in the subcortical areas of the brain). However, we now know the original dopamine hypothesis is not a complete explanation and dopamine levels in other brain areas are too low rather than high. If this is true, then most antipsychotics should not work. There are also questions about the effectiveness.
This means that at least some antipsychotics may not be the best treatment - some other factors are involved in their success.